About the origin of chronic pain
The complete article has been offered to "Medical Hypothesis", waiting for review: 29 th november 2017 in Open Access.
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Here the abstract as a preview.
CRPS= Complex regional pain syndrome PGE=Prostaglandin E1 and E2
Conclusion: It is possible for chronic pain to be detected by infrared Thermography and to be tested for the CRPS risk. There exists a pharmaceutical possibility for treatment since 30 years with pentoxifylline. The drug blocks a specific inflammatory protein: TNF-alpha.
Abstract Hypothesis: Chronic pain without a detectable substrate and CRPS are part of the same inflammatory disease process and differ only in its process phase.
Chronic pain can be seen as a chronic inflammation without the classical features rubor, calor and tumor. As the result of a biochemical transition, the clinical picture of a cold inflammation can change into a virulent situation that shows all the characteristics of an inflammation: CRPS. The transition that may cause this was already described by Horrobin and Manku in 1977, but not recognised as such. The transition itself consists of a bell-shaped dose-effect curve for prostaglandins. The sensitivity can be increased or decreased by prostaglandins that have also been described but show a plateau in the dose-effect curve.
The background of the thought process was published earlier as: CRPS: A contingent hypothesis with prostaglandins as crucial conversion factor Med. Hypoth., Elsevier, 2015. The present article is a practical elaboration of the former publication which integrates chronic pain without a detectable substrate and CRPS in the same pathogenic process.
The effect of the biochemical process can be observed with infrared imaging and can be biochemically analysed. Treatment has already been available for 30 years and its progress can be followed and measured. This article addresses the disease process and its phases in a process-oriented medical way. The hypothesis is supported by much evidence, the collection of which is still incomplete. This article provides an applicable model suitable for further pure scientific research as well as a practical pursuit of therapeutic initiatives. It is also an ode to the impressive and significantly underestimated research conducted by Horrobin and Manku in 1977.
Conclusion: Chronic pain and CRPS overlap each other and both develop from an inflammatory accident resulting from trauma, fracture or haematoma. Chronic pain (the kick off) comes first and CRPS (the knockdown) follows. It can explain why CRPS occurs after relatively small injuries.
Consequently, the treatment of chronic pain should be focused on blocking the target sites of PGE and selective inhibition of PGE production and/or a selective increase of the PGE concentration and/or blocking of cytokines to which PGE tends to bind. A forty-year-old pharmaceutical - with a proven positive effect on chronic pain as well as on early CRPS - could be studied again to see if it has pharmacological properties leading to the effects mentioned above. To prevent the development of CRPS after relatively simple surgical procedures, infrared thermography should be used to examine the presence of chronic pain syndrome in the area for surgery and to test the surgery-induced propensity to develop CRPS. Finally, the above-mentioned pharmaceutical can be administered as preventive preoperative treatment to patients in whom a risk of CRPS has been established, but who nevertheless need surgery.
Published on 20/01/2018 by Henk